title: The over-expression of Pim-2 promote the tumorigenesis of prostatic carcinoma through phosphorylating eIF4B.
abstract: BACKGROUND
  Cell experiments have found Pim-2 may take part in the tumorigenesis of prostatic carcinoma (PCA). More direct evidences are needed, and the detailed anti-apoptotic mechanism of Pim-2 in PCA cells is still unknown.
  
  
  METHODS
  Pim-2 expression levels were compared between benign prostatic hyperplasia (BPH) tissues and PCA tissues using real time PCR and Western blot, respectively. Then Pim-2 expression levels were detected in PCA cell lines DU-145 and LNCaP, as well as in nontumorous prostatic epithelial cell lines RWPE-1 and PNT1a, using real time PCR and Western blot, respectively. The co-expression of Pim-2 and eukaryotic initiation factor 4B (eIF4B) was examined by immunofluorescence cytochemistry using laser scanning confocal microscope. Finally, Pim-2 SiRNA was transfected into DU-145 cells and Pim-2 was transfected into RWPE-1 cells, and the level of Pim-2 and phosphorylated eukaryotic initiation factor 4B (p-eIF4B) were detected, as well as the apoptosis rate.
  
  
  RESULTS
  The Pim-2 mRNA and protein level were significantly higher in PCA tissues than those in BPH tissues. The Pim-2 mRNA and protein level in DU-145 and LNCaP cells were significantly higher than those in RWPE-1 and PNT1a cells. Pim-2 and eIF4B could co-express in DU-145 cells. Pim-2 level determined the phosphorylation level of eIF4B and the apoptosis rate of prostatic cells. The higher Pim-2 expressed, the more eIF4B phosphorylated, then the less cell got apoptosis, and vice versa.
  
  
  CONCLUSIONS
  Pim-2 was over-expressed in PCA cell lines and tissues. It may inhibit the apoptosis of PCA cells through phosphorylating eIF4B, thus promote the tumorigenesis of PCA.
authors.affiliation: Department of Urology, The First Affiliated Hospital of Chongqing Medical University, PR China.
authors.forename: Ke
authors.initials: K
authors.lastname: Ren
authors.forename: Xin
authors.initials: X
authors.lastname: Gou
authors.forename: Mingzhao
authors.initials: M
authors.lastname: Xiao
authors.forename: Ming
authors.initials: M
authors.lastname: Wang
authors.forename: Chaodong
authors.initials: C
authors.lastname: Liu
authors.forename: Zhaobing
authors.initials: Z
authors.lastname: Tang
authors.forename: Weiyang
authors.initials: W
authors.lastname: He
mesh_terms: D017209:Apoptosis; D002277:Carcinoma / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D045744:Cell Line, Tumor; D002471:Cell Transformation, Neoplastic / Q000235:genetics / Q000378:metabolism*; D039642:Eukaryotic Initiation Factors / Q000378:metabolism*; D006801:Humans; D008297:Male; D010766:Phosphorylation; D011467:Prostate / Q000378:metabolism* / Q000473:pathology; D011470:Prostatic Hyperplasia / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D011471:Prostatic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
chemical_list: D039642:Eukaryotic Initiation Factors; C490587:PIM2 protein, human; D011518:Proto-Oncogene Proteins; D012333:RNA, Messenger; C031799:eIF-4B; D017346:Protein Serine-Threonine Kinases
keywords: Pim-2; apoptosis; eIF4B; phosphorylation; prostatic carcinoma